This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The Acquired Immunodeficiency Syndrome (AIDS) is caused by a virus called the human immunodeficiency virus (HIV) and has resulted over the last 25 years in millions of death worldwide. The early phase of the infection is crucial in the eventual progress toward AIDS. Soon after entering the body, HIV rapidly spreads to the lymph nodes and others organs where it makes many millions of copies of itself. If the virus could be well contained at the beginning, the infected person would develop AIDS only after many years while a person with rapid expansion of the virus in the first days of infection would develop AIDS much sooner. Despite recent progress in our understanding of Human Immunodeficiency Virus disease the actual mechanisms responsible for controlling the replication of the virus in the infected host remain poorly understood. CD4+ T cell depletion and the progression of HIV-1-related diseases are progressive in adults infected with HlV-L Some of the reasons why adults are able to longer survive over the time of the infection may be due to differences in the host immune control of virus replication such as the stronger presence of CD8 cytotoxic T lymphocytes (or "killer T lymphocytes) and a better neutralizing antibody response, that have been shown to inhibit HIV replication. Animal studies can help address critical questions that cannot be answered in human studies, in computer models or laboratory dishes. Most animal AIDS research is conducted with monkeys. Some monkeys are infected with SIV, a virus very similar to HIV that causes an AIDS-like disease. The similarities between SIV and HIV allow scientists to test theories, vaccines, and medications that could otherwise never by tested. In collaboration with Dr. Leonidas Stamatatos from the Seattle Biomedical Research Institute (SBRI, Seattle WA), we will investigate the development of immunity to the virus longitudinally to determine how the body learns to fight SlV. We will particularly investigate the generation of virus-specific neutralizing antibodies and cellular immune responses such as the CD8 cytotoxic T lymphocyte responses in an effort to correlate these responses with control of virus concentration in the plasma. With this study, we are expecting to see an increased production of anti-virus neutralizing antibody responses and strong anti-viral cell responses that will mimic the immune responses observed during HIV infection in patient.